ADAMTS1, also known as METH1, is a matrix metalloprotease. It has angioinhibitory properties, binds to VEGF and dampens VEGFR2 phosphorylation, with both its binding and catalytic domains likely required for antiangiogenic/antitumor activities [1]. It is also involved in many physiological and pathological conditions, such as tumorigenesis, metastasis, and ovulation [5,6].

In glioma, ADAMTS1 is highly expressed, correlated with malignancy grade and prognosis. Its knockout suppresses intracranial orthotopic xenograft growth and prolongs survival in mice, likely by affecting the Notch1-SOX2 signaling pathway in glioma stem cells [2].

In renal cell carcinoma, elevated ADAMTS1 is associated with poor prognosis. Manipulating ADAMTS1 affects cell anoikis through the mitochondrial pathway. A cyclic axis of ADAMTS1-VCAM-EGFR drives anoikis resistance and invasion [3].

In non-small cell lung cancer, ADAMTS1 promotes cell proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) by regulating TGF-β [4].

In polycystic kidney disease, loss of Pkd1 increases Adamts1 mRNA expression, leading to versican cleavage, macrophage accumulation, and cyst growth. Deletion of both Adamts1 and Pkd1 reduces these effects and improves kidney function [7].

In conclusion, ADAMTS1 plays diverse and significant roles in multiple biological processes and diseases. Through gene knockout models in mice, its functions in tumorigenesis, metastasis, and cyst expansion in polycystic kidney disease have been well-demonstrated, providing valuable insights into the underlying mechanisms and potential therapeutic targets for these diseases.